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Updated: Mar 16, 2026

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
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Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions

Published on: August 2, 2018

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Mitogen-Activated Protein Kinases and Hypoxic/Ischemic Nephropathy

Fengbao Luo1, Jian Shi, Qianqian Shi

  • 1Department of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|August 22, 2016
PubMed

Insights

Hypoxia/ischemia damages kidneys, but signaling pathways remain unclear. This review details how mitogen-activated protein kinases (MAPKs) mediate kidney responses to hypoxic/ischemic stress in various kidney diseases.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pathophysiology

Background:

  • Tissue hypoxia/ischemia is a key factor in stroke, heart attack, kidney disease, and cancer.
  • Kidneys are particularly vulnerable to hypoxic/ischemic injury due to high oxygen demand and limited supply.
  • Reduced renal oxygen is implicated in acute kidney injury, chronic kidney disease, and kidney cancer.

Purpose of the Study:

  • To explore the poorly understood signaling mechanisms by which hypoxia affects cellular behavior in the kidney.
  • To review the differential roles of mitogen-activated protein kinases (MAPKs) in renal responses to hypoxic/ischemic stress.

Main Methods:

  • Literature review focusing on recent studies, including the authors' own research.
  • Analysis of signaling pathways involving MAPKs (ERK1/2, JNK, p38, ERK5) in hypoxic/ischemic conditions.
  • Discussion of MAPK involvement in the pathophysiology of acute kidney injury, chronic kidney diseases, and renal carcinoma.

Main Results:

  • Mitogen-activated protein kinases (MAPKs) are crucial signal-transducing enzymes activated by hypoxia/ischemia.
  • Four major MAPK families (ERK1/2, JNK, p38, ERK5) are differentially involved in renal responses to hypoxic/ischemic stress.
  • MAPKs play significant roles in the cellular changes associated with kidney injury and disease.

Conclusions:

  • Understanding MAPK signaling is critical for deciphering hypoxia's impact on kidney health and disease.
  • MAPK pathways represent potential therapeutic targets for mitigating hypoxic/ischemic kidney damage.
  • Further research into MAPK regulation is needed to address acute kidney injury, chronic kidney disease, and renal cancer.

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